Fetal Alcohol Spectrum Disorder (FASD) is an umbrella term that refers to the continuum of neurobehavioral and physiological impairments resulting from maternal alcohol consumption during pregnancy. Of the cognitive, physiological and behavioral impairments associated with prenatal alcohol exposure (PAE) documented in the clinical and pre-clinical literature, lifelong social behavior deficits serve as a unifying feature across the entire continuum of Fetal Alcohol Spectrum Disorders (FASD). Impaired social behavior in individuals with FASD has widespread implications for other domains and may contribute to difficulties within the school environment, social rejection, trouble with the law, and later mental health problems. PAE-related social behavior deficits emerge early in development and become more pronounced prior to and during adolescence, a critical period of development during which significant behavioral, cognitive, and physiological changes occur, including onset of puberty, making adolescence a unique period of increased vulnerability to social behavior dysfunction. However, because of the considerable overlap in the characteristics of FASD and other childhood disorders with social behavior impairments ? including autism spectrum disorder (ASD) ? reaching a definitive diagnosis presents a challenge for the clinical community. Indeed, it has been suggested that the difficulty in identifying individuals affected by FASD has led to an underestimation of its already high prevalence (2-5%) in the general population. The relevance of the current research proposal relies on the need for establishing a more specific social neurobehavioral profile that could support the development of specific strategies for earlier diagnoses and more targeted interventions for FASD. Previous pre-clinical and clinical research suggests that PAE affects brain areas and alters neurotransmitters shown to support social behavior, including the prefrontal cortex, amygdala, and hypothalamus, as well as the oxytocin and vasopressin neurotransmitter systems. Accordingly, the present proposal will characterize social behavior and its underlying neural correlates using a well-established animal model of moderate PAE. We will test the hypothesis that PAE results in social behavior impairments (Aim 1) that result from altered development of the OT/AVP systems (Aim 2). In addition, because the clinical and preclinical literature support a role for oxytocin treatment in enhancing aspects of social behavior in healthy individuals as well as in ameliorating social behavior deficits associated with ASD, frontotemporal dementia, and schizophrenia, we also propose to investigate oxytocin administration as an intervention for rescuing social behavior deficits following PAE (Aim 3). The proposed studies will provide further insight into mechanisms underlying the effects of PAE on social behavior, and suggest possible approaches for attenuation of such deficits.